Evidence map›Paper›PMID 15452351›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Restoration of an absent G1 arrest and protection from apoptosis in embryonic stem cells after ionizing radiation.

Yiling Hong, Peter J Stambrook

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

115 citing papers in PubMed, 246 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Embryonic Stem Cell-Specific Responses to DNA Replication Stress.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Repetitive Sequence Stability in Embryonic Stem Cells.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Retina stem cells, hopes and obstacles.World journal of stem cells · 2021
    Review
  13. Review
  14. Stem cells and development · 2021
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Yiling HongDepartment of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, OH 45267, USA.
Peter J Stambrook
National Institutes of Health · USUniversity of Cincinnati Medical Center · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI YADAV, JAGJIT S · 1992 to 2022
$35.4M
Plk3 variants in transgenic mice and MEFsU01ES011038 · NIEHS · UNIVERSITY OF CINCINNATI · PI STAMBROOK, PETER J. · 2001 to 2006
$6.7M
PPK: Radiation Response and Cell ProliferationR01CA090934 · NCI · UNIVERSITY OF CINCINNATI · PI STAMBROOK, PETER J. · 2002 to 2006
$1.5M
NCI NIH HHS R01 CA090934NCI NIH HHS R01 CA 90934NIEHS NIH HHS ES 06096NIEHS NIH HHS P30 ES006096NIEHS NIH HHS U01 ES011038NIEHS NIH HHS U01 ES 11038
6 · The paper itself

Abstract

Response to DNA damage and cell-cycle regulation differ markedly between embryonic stem (ES) cells and somatic cells. ES cells require exquisitely sensitive mechanisms to maintain genomic integrity and do so, in part, by suppressing spontaneous mutation. Spontaneous mutation frequency in somatic cells is approximately 10(-4) compared with 10(-6) for ES cells. ES cells also lack a G(1) checkpoint and are hypersensitive to IR and other DNA-damaging agents. These characteristics facilitate apoptosis and the removal of cells with a mutational burden from the population, thereby keeping the population free of damaged cells. Here, we identify signaling pathways that are compromised and lead to a natural absence of aG(1) arrest in ES cells after DNA damage. The affected pathways are those mediated by p53 and p21 and by ATM, Chk2, Cdc25A, and Cdk2. In ES cells, Chk2 kinase is not intranuclear as in somatic cells but is sequestered at centrosomes and is unavailable to phosphorylate Cdc25A phosphatase and cause its degradation. Although ectopic expression of Chk2 does not rescue the p53/p21 pathway, its expression is sufficient to allow it to phosphorylate Cdc25A, activate downstream targets, restore a G(1) arrest, and protect the cell from apoptosis.

Indexed as

AnimalsApoptosiscdc25 PhosphatasesCells, CulturedCentrosomeCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p21CyclinsDNA DamageFibroblastsG1 PhaseMicePhosphorylationProtein Serine-Threonine KinasesRecombinant Fusion ProteinsStem CellsCdc25a protein, mousecdc25 PhosphatasesCdkn1a protein, mouseCheckpoint Kinase 2Chek2 protein, mouseCyclin-Dependent Kinase Inhibitor p21CyclinsProtein Serine-Threonine KinasesRecombinant Fusion ProteinsTubulinTumor Suppressor Protein p53

Identifiers

PMID15452351
PMCPMC521944
OpenAlexW2030071293

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.